1. Field of the Invention
The present invention relates to preventing and treating atrial fibrillation. More particularly this invention relates an apparatus and method temporarily used to prevent and/or treat atrial rhythm disturbances in postoperative cardiac patients.
2. Description of the Related Art
Atrial fibrillation is the most common postoperative cardiac rhythm disturbance, occurring in about 30–40% of all adult cardiac surgery patients. In addition, atrial fibrillation often induces hemodynamic instability and/or increases thromboembolic events. As a result, the high incident rate of atrial fibrillation is the leading cause of prolonged hospitalization after cardiac surgery. Further, the cost associated with this prolonged stay is high both from a viewpoint of the amount of money the stay costs the patient (or his insurance carrier) and from the viewpoint of the patient's lost ability to earn money through work.
Paradoxically, despite the numerous preventive improvements and measures that have arisen in surgical/cadiopulmonary bypass techniques, the incident rate of atrial fibrillation has increased in recent years. Although many preoperative and postoperative factors have been implicated, the precise mechanism responsible for the high incidence of atrial fibrillation in postoperative patients remains unknown.
In response to postoperative atrial fibrillation, current practice dictates pharmacological treatments and/or electrical shock conversion. Treatment of atrial fibrillation pharmacologically often fails and requires electrical shock conversion. In addition, maintaining the sinus rhythm after successful carioversion has proven to be quite difficult and, therefore, the recurrent rate is extremely high without systemic administration (orally or intravenously) of anti-arrhythmic drugs. For this reason, it is mandatory to administer anti-arrhythmic drugs for at least the recovery period. However, such systemic administration of drugs can be associated with significant side effects.
Intravenous procainamide is often used since it can reach therapeutic levels rather rapidly. However, procainamide can cause ventricular depression, hypotension, prolongation in the QT portion of the electrocardiogram, and/or ventricular fibrillation. As a result, careful monitoring of the procainamide serum levels is required. Further, maintaining optimum serum levels is difficult. Similarly, rapid intravenous infusion of amiodarone may cause significant ventricular depression/bradycardia. As a result, it is recommended to build the therapeutic level of amiodarone slowly, i.e., by taking between about 24 and about 48 hours. In addition, other long-term side effects of amiodarone may include injury to the lungs, thyroid, skin, and/or nervous system.
The undesirable systemic side effects from these drugs stem from the relatively high circulating levels of the drugs which needed are to raise their concentration in the atrial tissue. Therefore, it is desirable to deliver drugs to the atrial tissues without administering the drugs systemically. If the drugs were delivered directly to the atrial tissue, only a fraction of the systemic dose of the drugs would be needed to adequately raise their concentration in the atrial tissue, thereby achieving anti-atrial fibrillation effects without inducing systemic side effects. Procainamide is well known to infiltrate tissue readily and amiodarone is a lipophylic substance and is expected to infiltrate atrial tissue as well as procainamide. Ayers et al. demonstrated the effectiveness in suppressing atrial fibrillation using amiodarone instilled into a canine's pericardial sac. J. Cardiovascular Electrophysiology, vol. 7, no. 8, (August, 1996).
It is possible, of course, to deliver drugs directly to the pericardial sac after transvenously passing a catheter to the right atrium and thereafter transatrially puncturing the atrial wall, thereby providing access to the pericardial sac. See, e.g., U.S. Pat. Nos. 5,269,326 and 5,968,010. However, these approaches are very invasive and technically difficult and, therefore, carry significant risks. For this reason, systemic pharmacological treatments, with and without external electric shock, remains the preferred method of addressing atrial fibrillation in patients recovering from cardiac surgery.
Hemodynamic instability from atrial fibrillation or failure of pharmacological treatment of atrial fibrillation mandates electric shock defibrillation. Conventional external electric defibrillation procedures require high electrical energy (i.e., on the order of 100–300 joules) and, as a result of the intense shock and patient discomfort associated therewith, are preferably delivered after general anesthesia or deep sedation, both of which are time consuming procedures. In addition, as a result of the necessary anesthesia or sedation, external shock may require the presence of an anesthesiologist, a cardiologist, and an intensivist. Finally, the procedure itself is not without substantial risk; the human cost associated with external shock can include disturbing cardiac stability to the point where the patient may die.
Rapidly converting atrial fibrillation back to sinus is known to reduce the predisposition for intractable/additional episodes of atrial fibrillation. Implantable atrial cardioconverters (“IACs”), at least in theory, are an excellent device for detecting and rapidly converting atrial fibrillation. Further, IACs have been introduced to manage chronic atrial fibrillation and have proven to be safe and effective.
The standard lead configuration for IACs delivers a shock between electrodes in the right atrial appendage and the coronary sinus. As a result of this configuration, the posterior of the left atrium is exposed to the lowest shock and, therefore, often yields the lowest potential gradient in this region. Further, the lowest gradient often yields the earliest activation leading to an unsuccessful shock. To prevent this problem, IACs deliver about 3 to about 6 joules of energy, which may cause noticeable discomfort.
Unfortunately, associated with IACs are the following drawbacks: (a) discomfort from the shock provided by the device which is exacerbated by the frequent rate at which the shocks are administered; (b) a poor cost/effectiveness ratio; and (c) technical problems associated with the device which can not be readily addressed due to its being permanently implanted. As a result, IACs are no longer being used for chronic atrial fibrillation, unless coupled with an automated ventricular converter. Recently, an implantable atrial defibrillation (the Syncrus system of the Guidant Corporation) has been introduced for postoperative atrial fibrillation. However, this implantable atrial converter, which uses bi-atrial wires, requires a higher range of energy (e.g., 3–10 joules) for a successful cardioversion and, therefore, causes similar discomfort as in the aforementioned IAC.
There have been several previous improvements to treat postoperative atrial fibrillation. A first example involves covering more surface area of the atrium with the electrode (i.e., the electrode either winds around the surface of the atrium or divides into multiple wires each of which is directed toward a different portion of the surface area of the atrium). See, e.g., U.S. Pat. Nos. 5,741,322, 5,849,033, 5,928,278, 6,152,955, 6,324,435, 6,330,481, 6,385,491, 6,463,335, and U.S. patent application Publication 2002/0035388. By covering more of the atrial surface area, a more uniform shock may be applied to the atrium thereby increasing the likelihood of a successful shock.
In an attempt to address the lack of uniformity in the potential gradient, the electrodes in the aforementioned patents and patent application have been incorporated into pads which cover a greater portion of the atrial surface area. In addition, these pads may be bioabsorbable. See, e.g., U.S. Pat. Nos. 5,849,033, 6,330,481, 6,324,435, 6,385,491, 6,463,335, and U.S. patent application Publication 2002/0035388. By housing the electrode in a bioabsorbable pad, the electrode can easily be removed by pulling it through the patient's chest wall after the pad is absorbed thereby eliminating the need to open the chest cavity a second time. Unfortunately, however, the pads are bulky, present adhesion problems (due to the rounded shape of the heart and due to the fact that the heart's size continuously expands and contracts), and may interfere with the beating of the heart by inhibiting the ability of the atrium to expand.
Electrode pads have also been used to deliver time-release quantities of antiarrhythmic drugs. See, e.g., U.S. Pat. No. 6,385,491 and U.S. patent application Publication 2002/0035388. Unfortunately, the amount of drug delivered according to these methods is not controllable, i.e., the drug type, timing, and dosage is predetermined; the drug type and/or dosage can not be increased or decreased in response to changes in a patient's condition.
Accordingly, what is needed is a new method and apparatus which: (a) can successfully defibrillate an atrium while delivering a quantum of energy that a conscious and non-sedated patient will either not notice or easily tolerate; (b) is able to deliver antiarrhythmic medication directly to the atriums which will eliminate (or at least minimize) the aforementioned side effects caused by systemic exposure to high concentrations of antiarrhythmic drugs; and/or (c) has the ability to control drug delivery directly to the atriums in terms of drug type, timing, and/or dosage.